Current conceptions of[unreadable] sepsis-induced multiple organ dysfunction invoke a biphasic time course in[unreadable] which early overexpression of proinflammatory responses initiated by TNFa[unreadable] and members of the its superfamily including Fas (Apo-1, CD95) are followed[unreadable] by a secondary state of immunosuppression and susceptibility to infectious[unreadable] complications. TNFa- and Fas-mediated necrosis and apoptosis both result in[unreadable] cell death during sepsis. However, the balance between these two processes[unreadable] may critically determine the extent and progression of initial inflammation[unreadable] if the release of phlogistic constituents following necrotic cellular death[unreadable] is disproportionately enhanced. Apoptotic cell death may limit the degree[unreadable] of otherwise inevitable TNFa/Fas ligand (FasL)-mediated necrosis, even[unreadable] though apoptotic cell losses in the bone marrow, thymus, and lymph nodes may[unreadable] compromise host defense. Although important, the determinants of[unreadable] proinflammatory vs. apoptotic sequelae in response to increased production[unreadable] of TNFa and FasL, the specific cell surface receptors involved, and the[unreadable] exact signal transduction pathways are poorly understood at the whole animal[unreadable] level.